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Published February 15, 2001 | public
Journal Article

Expression of EphrinB2 Identifies a Stable Genetic Difference Between Arterial and Venous Vascular Smooth Muscle as Well as Endothelial Cells, and Marks Subsets of Microvessels at Sites of Adult Neovascularization


The transmembrane ligand ephrinB2 and its receptor tyrosine kinase EphB4 are molecular markers of embryonic arterial and venous endothelial cells, respectively, and are essential for angiogenesis. Here we show that expression of ephrinB2 persists in adult arteries where it extends into some of the smallest diameter microvessels, challenging the classical view that capillaries have neither arterial nor venous identity. EphrinB2 also identifies arterial microvessels in several settings of adult neovascularization, including tumor angiogenesis, contravening the dogma that tumor vessels arise exclusively from postcapillary venules. Unexpectedly, expression of ephrinB2 also defines a stable genetic difference between arterial and venous vascular smooth muscle cells. These observations argue for revisions of classical concepts of capillary identity and the topography of neovascularization. They also imply that ephrinB2 may be functionally important in neovascularization and in arterial smooth muscle, as well as in embryonic angiogenesis.

Additional Information

© 2001 Academic Press. Under an Elsevier user license. Received for publication August 11, 2000; Revised September 28, 2000; Accepted September 28, 2000; Published online January 19, 2001. We thank Shirley Pease for management of transgenic animals, Gabriele Mosconi for laboratory management, D. Panigrahy for assistance with tumor implantation, and Scott Gaspard and Hieu Phan for technical assistance. We also thank George Yancopoulos for calling our attention to the expression of ephrinB2 in the vaso vasorum. This work was supported in part by a grant from the American Heart Association to D.J.A. and the National Heart, Lung and Blood Institute (R37-HL51150 and P50-HL56985, to M.A.G.). S.-I.H. is the recipient of a Japan Heart Foundation Research Abroad Award. D.J.A. is an Investigator of the Howard Hughes Medical Institute.

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